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Mild endotoxemia, NF-κB translocation, and cytokine increase during exertional heat stress in trained and untrained individuals

Par Conseil national de recherches du Canada

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DOITrouver le DOI : https://doi.org/10.1152/ajpregu.00917.2007
AuteurRechercher : ; Rechercher : ; Rechercher : ; Rechercher :
FormatTexte, Article
Sujetsplanchnic permeability; immune function; blood volume; cardiovascular/thermoregulatory strain; flow cytometry
Résumé
This study examined endotoxin-mediated cytokinemia during exertional heat stress (EHS). Subjects were divided into trained [TR; n=12, peak aerobic power (VO2peak)=70+/-2 ml.kg lean body mass(-1).min(-1)] and untrained (UT; n=11, VO2peak=50+/-1 ml.kg lean body mass(-1).min(-1)) groups before walking at 4.5 km/h with 2% elevation in a climatic chamber (40 degrees C, 30% relative humidity) wearing protective clothing until exhaustion (Exh). Venous blood samples at baseline and 0.5 degrees C rectal temperature increments (38.0, 38.5, 39.0, 39.5, and 40.0 degrees C/Exh) were analyzed for endotoxin, lipopolysaccharide binding protein, circulating cytokines, and intranuclear NF-kappaB translocation. Baseline and Exh samples were also stimulated with LPS (100 ng/ml) and cultured in vitro in a 37 degrees C water bath for 30 min. Phenotypic determination of natural killer cell frequency was also determined. Enhanced blood (104+/-6 vs. 84+/-3 ml/kg) and plasma volumes (64+/-4 vs. 51+/-2 ml/kg) were observed in TR compared with UT subjects. EHS produced an increased concentration of circulating endotoxin in both TR (8+/-2 pg/ml) and UT subjects (15+/-3 pg/ml) (range: not detected to 32 pg/ml), corresponding with NF-kappaB translocation and cytokine increases in both groups. In addition, circulating levels of tumor necrosis factor-alpha and IL-6 were also elevated combined with concomitant increases in IL-1 receptor antagonist in both groups and IL-10 in TR subjects only. Findings suggest that the threshold for endotoxin leakage and inflammatory activation during EHS occurs at a lower temperature in UT compared with TR subjects and support the endotoxin translocation hypothesis of exertional heat stroke, linking endotoxin tolerance and heat tolerance.
Date de publication
Maison d’éditionAmerican Physical Society
Dans
  • AJP : Regulatory, Integrative and Comparative Physiology 295, nº 2 : R611–R623.
Langueanglais
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Numéro NPARC23001234
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Identificateur de l’enregistrementb0eac582-8202-4b41-94b3-64ccbd36f3b2
Enregistrement créé2017-01-09
Enregistrement modifié2020-06-02
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